This page is part of the site called Surgical Pathology of the Canine Male Reproductive Tract

Dr Rob Foster

OVC Pathobiology

University of Guelph

Pathology of the Canine Prostate

Table of Contents

Prostatic disease in general.

The similarity of the prostate of dogs and its diseases to that of humans has lead to an enormous number of studies into the pathology of the canine prostate. The major diseases will be detailed individually, with this section limited to those studies of a more general or clinical nature.Many authors have given an overview of prostate diseses (O'Shea 1962, Hornbuckle et al 1978, Basanti and Finco 1986, Olson et al 1987, Krawiec and Helfin 1992, 1994, Knecht, Johnston et al 2000).

O'Shea (1962) identified 3 stages in the life of a prostate - normal growth in the young adult, hyperplastic growth during middle age, and senile involution. 63% of 243 adult dogs had glandular hyperplasia. 10 out of 79 dogs over 11 years had senile involution. Castration causes atrophy. 3 dogs with retained testes all had normal prostates. Those dogs with Sertoli cell tumours (3 dogs) all had atrophy. 4 prostates had abscesses, 3 had squamous metaplasia.

Hornbuckle et al (1978) reviewed 140 cases of prostatic disease. 34 had complicated prostatic hyperplasia, 20 had chronic active prostatitis, 26 had acute prostatitis, 23 had a prostatic abscess, 15 had prostatic cysts, and 22 had carcinoma.

Krawiec and Helfin (1992) studies 177 dogs with prostatic disease. 33 had prostatitis, 27 had cysts, 13 had neoplasia, 11 had hyperplasia, 1 had paraprostatic cyst, and 1 had blastomycosis of the prostate. 90 had prostatic enlargement.

Teske et al (2002) found prostatic hyperplasia in 246 dogs (57.1%), prostatitis in 83 dogs (19.3%), and prostatic carcinoma in 56 dogs (13%).

Palmieri et al (2015) examined the prostates of 111 dogs from archival specimens and categorised them as having benign prostatic hyperplasia, squamous metaplasia, suppurative and non-suppurative prostatitis; prostatic inflammatory atrophy, high grade prostatic intraepithelial neoplasia, and prostatic carcinoma. They had 50 carcinomas.

In the Yager-Best Histovet files there are are 131 cases of hyperplasia, 71 carcinomas, 68 cases of prostatitis, 23 prostatic cysts, 14 cases of squamous metaplasia, and 5 prostatic abscesses.

Palmieri et al (2019) outlined the concensisi terminology of epithelial lesions of the canine prostate.



Basanti JA, Finco DR. (1986) Canine prostatic diseases. Vet Clin North Amer: Small Anim Pract. 16: 587-599.

Hornbuckle WE, MacCoy DM, Allan GS, Gunther R. (1978) Prostatic disease in the dog. Cornell vet. 68 (Suppl 7): 284-305.

Johnston SD, Kamolpatana K, Root-Kustritz MV, Johnston GR (2000) Prostatic disorders in the dog. Anim Reprod Sci. 60-61:405-415

Knecht CD () Diseases of the canine prostae gland (Part 1). Compend Contin Edu :385-391.

Krawiec DR (1994) Canine prostatic disease. J Amer Vet Med Assoc 204: 1561-1564.

Krawiec DR, Helfin D (1992) Study of prostatic disease in dogs: 177 cases (1981-1986). J Amer Vet Med Assoc 200: 1119-1122.

Olson PN, Wrigley RH, Thrall MA, Husted PW, (1987). Disorders of the canine prostate gland: pathogenesis, diagnosis, and medical therapy. Compend Contin Edu - Small Animal 9: 613-623.

O'Shea JD (1962) Studies on the canine prostate gland. 1 factors influencing its size and weight. J Comp Pathol 72: 321-331.

Palmieri C, Foster RA, Grieco V, Fonseca-Alves CE, Wood GA, Culp WTN, Murua Escobar H, De Marzo AM, Laufer-Amorim R. Histopathological Terminology Standards for the Reporting of Prostatic Epithelial Lesions in Dogs. J Comp Pathol 2019; 171: 30-37

Teske E, Naan EC, van Dijk EM, Van Garderen E, Schalken JA. (2002) Canine prostate carcinoma: epidemiological evidence of an increased risk in castrated dogs. Mol Cell Endocrinol. 197(1-2):251-255

Prostatic atrophy

Hormonal therapy and neutering

The prostate is under hormonal control with both estrogens and androgens contributing to size. The prostate undergoes atrophy when there is a reduction in hormone concentration. Castration causes atrophy, especially of the epithelial component. Dogs with sustentacular (Sertoli) cell tumours develop atrophy, but there is also a risk of development of squamous metaplasia (O'Shea 1962).

Cazzuli et al (2022) reported on the changes that occurs after castration. They did an ultrasound evaluation and serum testosterone and estrodiol. Their case numbers were normal animals castrated (8 animals) prostatic hyperplasia and castrated (9) and uncastrated (10). Testosterone and estrodiol concentration dropped from normal to 0 in 7 days. Volume and size decreased from normal for 60 days before leveling off.

Prostatic inflammatory atrophy

There are publications that describe changes in the prostate in inflammation that are the canine equivalant of the human disease of Prostatic inflammatory atrophy (PIA) this work is in its infancy and not fully evaluated. Atrophy occurs in chronic prostatitis and the epithelial changes in prostatitis will be mentioned below in the section on prostatitis.



Cazzuli G, Damián JP, Molina E, Pessina P. Post-castration prostatic involution: A morphometric and endocrine study of healthy canines and those with benign prostatic hyperplasia. Reprod Domest Anim. 2022; 57: 157-164.

Palmieri C, Foster RA, Grieco V, Fonseca-Alves CE, Wood GA, Culp WTN, Murua Escobar H, De Marzo AM, Laufer-Amorim R. Histopathological Terminology Standards for the Reporting of Prostatic Epithelial Lesions in Dogs. J Comp Pathol 2019; 171: 30-37


Prostatic hyperplasia (also called benign prostatic hyperplasia [BPH])

Canine prostates go through progressive changes with age. A prepubertal dog has a very small prostate, and with puberty, it increases in size to 'normal'. The size tends to reflect body size although the Scottish terrier is reported to have a prostate that is about 4 times the size of dogs of a similar size (O'Shea 1962) and Rhodesian Ridgebacks develop more hyperplasia than like sized dogs. About 63% of dogs develop progressive enlargement of the prostate with age after puberty (O'Shea 1962). Berry et al (1986) quantified the changes in the prostate in Beagle dogs and noted that with age, the prostate enlarges and maintains its structure. At an age beginning at about 2 years, some dogs developed benign prostatatic hyperplasia where the structure changed from the glands being simple tubular structures (glandular BPH) to what they called 'complex BPH' wherein the glands became nodular, irregular with atrophy and cyst formation.

The size can become large enough to cause clinical signs of faecal obstruction rather than urinary obstruction (as occurs in humans). The enlarged prostate hangs over the pelvic brim when the dog is in its normal quadrapedal position, but when the position for defaecation is assumed, the prostate is pulled by gravity into the pelvic inlet and with an increase in intraabdominal pressure, forms a 'ball valve' and compresses the colon. Some dogs develop 'senile atrophy' of the prostate (O'Shea 1962).

Now comes the 'eliphant in the room'. What then is a normal canine prostate and when is it truely hyperplastic? Noone has dealt adequately with this issue. In most circumstances we use 2 standard deviations above and below the mean as the reference range of normal. When is the prostate hyperplastic and when is it a normal age associated change? Still, publications continue without an adequate definition.

The increase in size is reported to be the result of increased interstitial tissue with the overall amount of epithelium not increasing in amount. The lumen of glands, however, increase in diameter with age (James and Heywood 1979, Lowseth et al 1990). Shain and Boesel (1978) examined the androgen receptor content of canine prostates and found that hyperplastic glands had a greater receptor content than normal, but there was no difference in the receptor content per cell, and there was no increase in testosterone. Moore et al (1979) found that estradiol enhanced androgen effects on the prostate by enhancing an androgen binding protein in the cytoplasm.

Wolf et al (2012) measured 17B estrodiol, testosterone, DHT, prolactin and relaxin in 77 dogs and found the E2: T concentration was higher in dogs with prostatic hyperplasia. Prolactin may be involved but relaxin did not appear to be so.

Berry SJ, Strandberg JD, Saunders WJ, Coffey DS. Development of canine benign prostatic hyperplasia with age. Prostate. 1986;9(4):363-73.

James RW, Heywood R. (1979) Age-related variations in the testes and prostate of beagle dogs. Toxicology. 12(3):273-279.

Lowseth LA, Gerlach RF, Gillett NA, Muggenburg BA. (1990) Age related changes in the prostate and testes of the beagle dog. Vet Pathol 27: 347-353.

Moore RJ, Qazak JM, Wilson JD. (1979) Regulation of cytoplasmic dihydrotestosterone binding in dog prostate by estradiol. J Clin Invest 63: 351-357.

O'Shea JD (1962) Studies on the canine prostate gland. 1 factors influencing its size and weight. J Comp Pathol 72: 321-331.

Shain SA, Boesel RW (1978) Androgen receptor content of the normal and hyperplastic canine prostate. J Clin Invest 61: 654-660.

Werhahn Beining F, Urhausen C, Wolf K, Schmicke M, Rohn K, Schuler G, Günzel-Apel AR. Rhodesian Ridgebacks have an increased risk to develop benign prostatic hyperplasia. Reprod Domest Anim. 2020; 55: 283-292.

Wolf K, Kayacelebi H, Urhausen C, Piechotta M, Mischke R, Kramer S, Einspanier A, Oei CHY and Gunzel-Apel A (2012) Testicular steroids, prolactin, relaxin and prostate gland markers in peripheral blood and seminal plasma of normal dogs and dogs with prostatic hyperplasia. Reprod Dom Anim 2012, 47: 261-266

Macroscopic changes

The hyperplastic prostate is said to be uniformly enlarged. It typically has a smooth capsular surface and the parenchyma is uniform. While it initially will be a round bilobed structure, as it attains a greater size, it will become elongate. It retains its bilateral uniformity, although as the hyperplasia becomes advanced this is less so.. It is usual for the glands to have an increased luminal diameter and this is variable from gland to gland. Many will become cystically distended to the extent that multiple 'cysts' will be visible on cut section.

Figure : Prostatic hyperplasia (right) compared to a 'normal' prostate of a pubertal dog. The bladder is ventral in each example.

Figure : Advanced prostatic hyperplasia in a dog.

Microscopic changes

Prostates from entire dogs have a characteristic appearance to the epithelium. The acini are small and are lined by a single layer of columnar epithelial cells that have prominent granules in the apical cytoplasm. The nuclei are basally located .With hyperplasia in some dogs or in some parts of the prostate, there is an increase in the diameter of the lumen of the acini. This increase is variable with some being very large and others normal. The epithelial cells are prominent and are large columnar cells with a prominent apical cytoplasm filled with eosinophilic globules. The interstitium is inapparent. In other areas there is a prominent interstitium that widely separates the acini. Even these acini will be distended. The smooth muscle of the capsule and trabeculae is often prominent and the cells hypertrophied. Inflammation is absent or minor and interstitial.

There are 2 general forms of hyperplasia - glandular and complex. Simple glandular hyperplasia is when there is hyperplasia with a normal arrangement of ducts and glands. The increase in size of each unit is uniform. Glands are often papillary and project into the lumens. Individual cells are hypertrophied with a prominent vaculoated cytoplasm with eosinophilic globules.

Complex hyperplasia is when there are regions of hyperplasia with a nodular appearance, variable cystic dilation of lumens and regions of atrophy and irregularly increased stroma. Interstitial inflammation is common.

Figure : Prostatic hyperplasia, with acinar dilation and prominent epithelial cells.

Figure : Prostatic hyperplasia with an increase in interstitium. Acini are distended.

Nodular hyperplasia (adenoma?)

Gilson et al (1992) report on a dog that had a large prostatic mass that was resected. Histologically it was a combination of glandular tissue and stroma, that was initially called an adenoma, but was then regarded as nodular hyperplasia.

Gilson SD, Miller RT, Hardie EM, Spaulding KA (1992) Unusual prostatic mass in a dog. J Amer Vet Med Assoc 200: 702-707.

Squamous metaplasia of the Prostate

Squamous metaplasia occurs when the glandular epithelium of the prostate becomes stratified squamous in type instead of the columnar epithelium normally present. The mechanism for the development of squamous epithelium involves the production of keratins by the basal cells. The most dramatic forms of squamous metaplasia occur with exposure to estrogens or in feminizing syndromes. Irritation (from inflammaton) will also result in squamous metaplasia, but this is a subtle change and not as dramatic as with exposure to estrogens. Administration of estrogens (for prostatic disease!) or in dogs with testicular tumours and a feminisation syndrome is where it is mostly seen (O'Shea 1963).


Squamous metaplasia can be readily induced by administering estrogens to male dogs. In all animals, paracrine signals from the stroma define the epithelial type that will develop. It will also define the arrangement of the epithelium, including whether the epithelium will form a gland or a cavity. The mesenchyme also defines the function of the epithelium such as what proteins will be produced. This whole interaction involves epithelial feedback and regulation (reviewed by Cunha et al 2004). Steroid hormones regulate this interaction and in the the normal prostate, androgen receptor (AR) is an important factor. In estrogen induced squamous metaplasia, estrogen stimulates the ERalpha receptor, which is especially important in the stroma (the main ER of the epithelium is ERbeta). Using ERknockout mice, both stromal ERalpha and epithelial ERalpha must be present and stimulated to induce both proliferation and metaplasia. The stratified squamous cells acquire cyclooxygenase 2 activity as as result of estrogen stimulation.

Macroscopic findings.

The prostate can be variably affected so that no abnormalities may be detected grossly. The most severely affected though will be larger and have mulifocal pinpoint to miliary foci of white pasty material. Fibrosis can be dramatic also.

Microscopic findings

The histological changes of squamous metaplasia are those of dramatic replacement of the glandular epithelium with stratified squamous epithelium. The center of the acini are filled with laminations of keratin. The amount of keratin can be so great to cause enlargement of the acinus. The epithelium is well diffferentiated stratified squamous, with a basal layer, stratum spinosum and keratinization. Some acini will also have granulomatous and neutrophilic inflammation.

The squamous metaplasia that occurs secondary to prostatitis is subtle and there is marked accumulation of neutrophils and macrophages in the lumens, and some of the epidthelium is a thin layer of stratified squamous epithelium. Keratinization is unusual.

Cunha GR, Cooke PS, Kurita T (2004). Role of stromal-epithelial interactions in hormonal responses. Arch Histol Cytol 67(5):417-434.

Dore M, Chevalier S, Sirois J. (2005) Estrogen dependent induction of cyclooxygenase-2 in the canine prostate in vivo. Vet Pathol 42: 100-103.

O'Shea JD (1963) Squamous metaplasia of the canine prostate gland. Res Vet Sci 4: 431-434.

Prostatic neoplasia

It is believed (dogma) that prostatic neoplasia in dogs has no precancerous lesion. There does not appear to be a progression from nodular hyperplasia to adenoma to carinoma in situ to invasive carcinoma. In human prostate speak, this includes the 4 stages of Prostatic Intraepithelial Neoplasia (PIN). As such, the precancerous lesions of the first 3 stages of PIN are rare if they exist.


The only lesion reported that could be adenoma was considered by the authors to be nodular hyperplasia (see above)




Prostatic carcinomas occur in sexually intact and neutered dogs and there is little difference between them (Bell et al 1991), although Teske et al (2002) found an increase risk in castrated dogs. Tumours in castrated dogs tend to have pulmonary metastasis when diagnosed.

Although some consider this a common or frequent disease, Teske et al (2002) found that in out of 15,363 accessions of male dogs, 225 were diagnosed with prostatic disease. They indicate that the proportion of animals with each disease was similar so based on their graph 33 cases of their submissions were carcinoma. This would make the prevalence 0.2% of submissions. In terms of prostatic disease, carcinoma represented 12% of submissions.


Macroscopic changes

Prostates with neoplasia are highly variable in their gross appearance. Some, particularly those in neutered dogs, have very little change. Slight enlargement may be the only change. When sectioned, there is usually a central cavity with a fibrous wall, or focal white areas of necrosis. Sometimes the carcinoma tracks up the deferent ducts (Guerin et al 2012).

Figure : Prostatic carcinoma, neutered dog. Prostate is on the left and has a central cavity of necrosis. The bladder is central right.

At the other extreme is when the prostate is dramatically enlarged and greater than 10 cm in diameter. They tend to be multinodular, asymetrical, and often have adhesions to the surrounding tissues.

Figure :Prostatic carcinoma with marked enlargement and a multinodular appearance. The small structure on the left is a partially hidden bladder.

Microscopic changes

Histological changes in the prostate are typical of carcinoma. The phenotype is quite variable and many are mixtures of the individual types. Most have a very scirrhous appearance with large amounts of fibrous tissue and some have areas of necrosis. Most are not very challenging, unless there is obscuring inflammation. Compared to the range of prostate carcinoma of humans, the dog examples are mostly 'high grade'.

Normal prostates have a discontinious capsule through which protrudes glands of well differentiated cells. These should not be confused with invasion of a neoplasm. The presence of prostatic ducts with a transitional type of cell should not be mistaken for neoplastic change, and squamous metaplasia should be differentiated from squamous cell carcinoma.

If there is a 'typical' carcinoma, it is an invasive lesion that replaces and obliterates existing parenchyma. The cells are arranged in large cavities with necrotic cells in the center. Others are cords, nests or individuals surrounded by fibrous tissue. Criterial of malignancy including anosocytosis, anisokaryosis, reduced nuclear to cytoplasmic ratio and a high mitotic count are present.


Histological classification

It is fair to say that histological classification of carcinoma of the prostate in dogs is a zoo. There are different approaches, beliefs and schemes. What is required is a detailed study of the disease in the dog and an agreed upon classification. The human approach - known as the WHO Classification is logical and worth considering for dogs. Unfortunately, some authors regard the canine disease to be acinar. Others think it is urothelial, others ductal. It is time for consistency.

In humans, about 90% of carcinomas are acinar adenocarcinomas. Urothelial carcinomas are a small percentage. They arise from the pelvic urethra, periurethral glands and proximal prostatic duct urothelium. A good resourse that provides definitions of each entity including Gleason Scoring is the American Urological Association which provides a great website with educational materials. Click on the link to go there.

Human classification

The WHO Classification of tumours of the prostate outlined by Humphreys et al (2016) is as follows:-

A. Epithelial tumours

      1. Acinar adenocarcinoma
        1. atrophic
        2. pseudohyperplastic
        3. microcystic
        4. foamy gland
        5. mucinous
        6. signet ring like
        7. pleomorphic giant cell
        8. sarcomatoid
      2. Prostate intraepithelial neoplasia high grade
      3. Intraductal carcinoma
      4. Ductal adenocarcinoma
        1. cribriform
        2. papillary
        3. solid
      5. Urothelial carcinoma
      6. Squamous neoplasms
        1. adenosquamous carcinoma
        2. squamous cell carcinoma
      7. Basal cell carcinoma

B. Neuroendocrine tumours

C. Mesenchymal tumours

D. Haematolymphoid tumours

E. Miscellaneous tumours

F. Metastatic tumors

A good resourse that provides definitions of each entity including Gleason Scoring is the American Urological Association which provides a great website with educational materials. Click on the link to go there.


Humphrey PA. Histological variants of prostatic carcinoma and their significance. Histopathology. 2012; 60: 59-74

Humphrey PA, Moch H, Cubilla AL, Ulbright TM, Reuter VE. The 2016 WHO Classification of Tumours of the Urinary System and Male Genital Organs-Part B: Prostate and Bladder Tumours. Eur Urol. 2016;70: 106-119.


Canine Classification

The classification of canine neoplasia requires some serious consideration, with definitions for each entity. Here is a historical perspective on classification of carcinomas of the prostate. Notice I dont use the term 'carcinoma of the prostate'. Until there is consensis about what is adenocarcinoma and what is urothelial carcinoma (the new term for transitional cell carcinoma), doubt will remain.

O'Shea (1968) classified 6 of 7 to be adenocarcinoma, while 1 was classified as a urothelial carcinoma.

Leav and Ling (1968) divided carcinomas into adenocarcinoma (intraalveolar and small acinar types) and undifferentiated adenocarcinoma (syncytial and descrete epithelial types).

Cornell et al (2000) examined 76 cases in detail and divided canine prostate carcinoma into adenocarcinoma, urothelial carcinoma, squamous carcinoma and mixed carcinoma, on morphological grounds. The criteria for each was lacking. The majority of theirs were considered mixed or adenocarcinomas.

LeRoy et al (2004) used the Leav and Ling (1968) classification. They compared carcinomas in the prostate with urothelial carcinomas of the bladder. Both had similar patterns.

Lai et al (2008) examined 20 cases and divided the carcinomas into micropapillary, cribriform, solid, sarcomatoid, small acinar/ductal and tubulopapillary patterns. They noted that mixed patterns occurred in 15 of 20 cases and all in the same cross section.

Palmieri et al (2014) had 50 carcinomas and 31 (62%) were of a single type, either small acinar/ductal, solid, cribriform (with or without comedonecrosis), or papillary (with or without comedonecrosis). The remainder (19 or 38%) were mixed with one or more of the patterns. These authors expanded the types of carcinoma of the prostate and their types were papillary, cribriform, solid, and small acinar/ductal types. They also noted sarcomatoid, signet ring, and mucinous types. Dogs with urothelial carcinoma of the bladder were excluded.

Ackers et al (2015) studied carcinomas of the prostate of 34 dogs using staining for androgen receptor, CK8 and CK18 for luminal cells and CK5 and CK14 for basal cells. They considered them all adenocarcinoma and identified 4 types of tumor - cribriform, solid, small acinar/ductal and micropapillary types.

de Brot et al (2022) reported on the division of their 41 cases into adenocarcinoma (10/41), urothelial carcinoma 21/41), and mixed carcinoma (9/41). p63 staining was positive in 24/40. The staining patterns for p63, HMWCK, Uroplakin III and NSE were reported by not consistent for histological classification. They had many cases with an intraductal component that they considered unique to their study; however carcinoma in situ is reported - as neoplasia within ducts in prostates with carcinoma.

So what is the bottom line with classification in my humble opinion (IMHO)?

  1. Urothelial carcinoma of the pelvic urethra and proximal prostatic ducts occur, and the patterns can be identical to those of adenocarcinomas.
  2. It makes more sense that dogs neutered as puppies are more likely to develop urothelial or ductal carcinomas.
  3. Location and growth habit of the carcinoma is important in differentiating urothelial from adenocarcinoma
  4. Until there is a prognostic difference identified between the various types, the generic term 'carcinoma of the prostate' or 'prostate carcinoma' be used (with prostate being a descriptive noun). Prostatic carcinoma is ok too.
  5. Many carcinomas have a mixed phenotype (as they do in humans).
  6. Subdividing carcinoma of the prostate into types is a research tool. Until better ways of defining urothelial and glandular types is available, the basic division of carcinomas should be Urothelial, mixed urothelial and adenocarcinoma, adenocarcinoma and squamous cell carcinoma.
  7. Terminology of the subtypes of adenocarcinoma and urothelial carcinoma should reflect the human terminology
  8. The terminology used in the review paper by Palmieri et al (2019) is a good start

Consensis classificiation based on Palmieri et al (2019) (yes I was involved)

1. Urothelial carcinoma:

  • solid,
  • papillary,
  • cribriform (with and without necrosis)

2. Adenocarcinoma:

  • simple tubular
  • papillary
  • cribriform
  • solid

3. Carcinoma with mixed urothelial and glandular phenotypes

de Brot S, Lothion-Roy J, Grau-Roma L, White E, Guscetti F, Rubin MA, Mongan NP. Histological and immunohistochemical investigation of canine prostate carcinoma with identification of common intraductal carcinoma component. Vet Comp Oncol. 2022; 20: 38-49.

Palmieri C, Foster RA, Grieco V, Fonseca-Alves CE, Wood GA, Culp WTN, Murua Escobar H, De Marzo AM, Laufer-Amorim R. Histopathological Terminology Standards for the Reporting of Prostatic Epithelial Lesions in Dogs. J Comp Pathol 2019; 171: 30-37



Figure : Prostate carcinoma

Figure : Prostate carcinoma

Figure : Prostatic carinoma



Grieco et al (2003) looked at 11 carcinomas - one squamous cell carcinoma, 7 adenocarcinomas and 3 undifferentiated. All stained with AE1/AE3 and with vimentin 3B4. 10 stained with CK8-12 (for luminal cells) and 6 coexpressed CK14 (for basal cells). They suggested that coexpresion of luminal and basal cell types indicate an epithelial stem cell phenotype.

Lai et al (2008) examined carcinoma of the prostate using HMWCK (CK 1, 5, 10 and 14), CK 5, CK7, CK14 and CK 18, uroplakin III, prostatic specific antigen and prostate specific membrane antigen. Of all 20 tumors examined, all stained for CK18, 17 for CK7, 13 for CK5, 12 for CK14 and uroplakin, 11 for HMWCK, 10 for PSMA and 8 for PSA. This compares with the staining characteristics of normal gland, prostatic duct and urothelium. In intact dogs, luminal acinar cells were all PSA and CK18+. 2 of 8 were CK7+. Basal acinar cells were HMWCK (2/8) + and CK5+ (5/8). Prostatic ducts were mostly CK18+ (8/8 for periurethral and 7/8 for peripheral duct), and all were negative for UPIII. 6/8 were positive for PSA. The luminal urothelium was UPIII (all), CK5 (all) PSA (6/8), CK5 (6/8) positive. basal urothelial cells were UPIII negative but most w ere HMWCK and CK5 positive. In castrated dogs (2 cases), the urethra was identical to the intact dogs. Only ducts were present in the prostate and they all stained for PSA, PSMA, and CK18. The periurethral tubules stained for CK7.

The origin of the various carcinomas has been debated for many years. Weaver (1981) indicated that it was impossible to differentiate primary prostatic carcinoma from transitional cell carcinoma. LeRoy et al (2004) attempted to use a less subjective method than morphological features by using techniques to identify cytokeratin 7 and arginine esterase, but could not differentate between the major types. There are no consistent immunohistochemical markers for prostatic carcinomas. As both cell types (glands) arise from a common progenitor, it is not surprising! Normal and hyperplastic prostate stains for Prostatic specific antigen (PSA), PSA protein (PSEP) and for Canine prostatic antigen.

In the 31 cases examined by McEntee et al (1987) only 8 stained for canine prostatic antigen, 2 stained form PSA and 3 stained for PSAP.

LeRoy et al (2007) investigated potential phenotypes of carcinoma of the prostate by comparing protein expression profiling. They examined carcinomas from 3 dogs and compared from 789 to 1305 proteins from these and from normal bladder and prostatic epithelia from 6 dogs. There was no clear similarity of protein expression between the neoplasms and normal tissues and it appeared as thought the protein expression of the neoplasms was different and unique to the protein expression of the normal tissues.

Lai et al (2008) wrote a series of papers that involved immunohistochemical staining of normal prostates from castrated and intact dogs, and from 20 dogs with spontaneous prostate tumours. 11 of these dogs were neutered and nine were intact. They stained the tissues with cytokeratins HMWCK, CK5, CK7, CK14, and CK18, uroplakin III, prostate specific antigen (PSA) and prostate-specific membrane antigen (PSMA). They classified the carcinomas into six groups: – solid, cribriform, micropapillary, sarcomatoid, small acinar/ductal and tubulopapillary. Eight of 20 stained with PSA, 10 of 20 stained with PSMA, 17 of 20 stained with uroplakin III, 12 with CK7, 11 of 20 stained with HMWCK, 13 with CK 5, 12 with CK 14 and 20 express CK 18. Their interpretation was that prostatic carcinomas most likely originate from collecting ducts and that the canine disease resembled human androgen refractory poorly differentiated carcinoma.

Ackers et al (2015) then examined the dogs reported by Palmieri et al (2014) and attempted to determine if the origin of the neoplastic cell was a basal, intermediate or luminal cell. This of course assumes that the carcinomas are adenocarcinomas, and arise in the glandular tissue. Their control tissue was acini of normal and hyperplastic prostates. They used basal cell markers (CK 5 and CK 14), luminal markers (androgen receptor, CK 8 and 18) and intermediate cells (of basal region CK5+ CK14, or intermediate cells of the luminal layer CK 5 and CK 18 coexpression). They could not consistently get p63 to work. They only selected the prostatic carcinomas with a single and not a mixed phenotype. The neoplasms had a variety of staining patterns. They found a predominance of staining as would be expected in luminal cell types (AR, CK8 and CK18). As with their previous paper, there was no indication of neuter status or the dogs.


        Basal cell Basal cell   luminal cell luminal cell ? acinar   urothelium
  Vimentin PanCK


(1, 5

CK5 CK14 CK7 CK8 CK18 AR PSA Uroplakin III
McEntee 1987                      
Greico et al (2003) 11/11 11/11   1/11 6/11   10/11        
Lai et al (2008)     11/20 13/20 12/20 17/20   20/20   10/20 12/20
Lai et al (2009)                 16/20    
Ackers et al (2015)       25/34 20/34   33/34 33/34 34/34    



Occurrence of metastatis:

Leav and Ling (1968) found metastases in 20 of their 20 dogs.

Cornell et al (2000) found metastasis in 80% of their 76 cases

Palmieri et al (2014) reported 12 out of 50 (24%) cases were metastatic.

Ravicini et al (2018) reported on 67 affected dogs. 60 were castrated and 7 were intact. 26 had metastasis - lymph nodes in 19, lungs in 10, and bone in 2. Median survival overall was 82 (7-752 days). With NSAIDS and chemotherapy, the MST was 106 days, and 51 days in dogs without therapy.


Location of metastasis

Palmieri et al (2014) reported that the common sites were lung, lymph node and kidney. No boney involvement was reported.

A diagnosis of prostate carcinoma in a dog carries an extremely poor prognosis. Many have metastasis at diagnosis - to 100% is reported. Many will develop metatasis unless they succumb to local disease first. Metastasis is to the lung and local lymph node, and about 7 to 14% have metastasis to bone, especialy the lumbar vertebrae and pelvis (Leav and Ling 1968, Durham and Dietze 1986, Cornell et al 2000).

Rodrigues et al (2011) suggests that vimentin expression by a prostatic carcinoma indicates a progression to a maligancy phenotype. They identified changes they considered to be prostatic inflammatory atrophy, prostatic intraepithelial neoplasia (PIN) and invasive carcinoma. Considering the dogma that canine prostates do not develop low and intermediate grade PIN and that the photomicrographs provided in the publication are not convincing, I suggest this be accepted with caution and that it requires substantiation. Positive staining for vimentin of the epithelial cells is known in prostatic carcinomas, and as all prostatic carcinomas are malignant (or are believed to be so), it is not surprising that this study found vimentin associated with a malignant phenotype.


There are no known causes, although there is a slightly increased risk in castrated dogs (Teske et al 2002). As already indicated, castration is not protective so the systemic hormonal environment does not appear to be important. Lai et al (2009) looked at this further and found that androgen receptors were less common in neoplastic prostatic tissue than in normal prostate. Postive staining was in the cytoplasm rather than the nucleus and there was no detectable mutations to DNA coding for the androgen receptor.
There are numerous studies outlining the distribution of estrogen receptors in canine prostates, and the intranuclear receptors are found in stromal cells and in the epithelial cells. Hyperplastic prostates have a similar distribution. Grieco et al (2006) found a loss of estrogen receptors in the stromal of all prostates including those with carcinoma. The main ER in the epithelium is ERBeta. In the more 'differentiated' tumours, ER was present but with less intense staining. Staining was reduced with the less differentiated tumours. The significance of this is yet to be established. Gallardo et al (2007) examined androgen receptor, estrogen alpha and beta, and progesterone receptor expression in prostatic specimens from dogs with prostatic hyperplasia, prostatatitis and neoplasia. Expression of these were less common in disease except for progesterone receptor, where more animals had expression in disease conditions.

Palmieri and Riccardi (2013) reported on the presence of the homeobox gene HOXA13 in normal, hyperplastic and neoplastic prostatic tissue and found it in all cases but much more prevalent in carcinoma of the prostate.

Prostatic intraepithelial neoplasia. It is widely believed that precursor lesions, such as low grade prostatic intraepithelial neoplasia (PIN), do not occur in dogs. High grade prostatic intraepithelial neoplasia is seen, and often in prostates with neoplasia. Waters and Bostwick (1997) report the presence of high grade prostatic intraepithelial neoplasia in dogs. They examined 35 prostates from dogs without clinical evidence of prostatic disease. They found high grade PIN in 1 of 13 dogs less than 4 years, and 6 of 11 dogs from 7 to 11 years old, and in 1 of 11 dogs that had been castrated. Waters et al (1997) found high grade PIN in19 of 29 prostates with carcinoma. Madewell et al (2004) examined canine prostates for high grade PIN. No examples were seen in 20 normal prostate glands or in 95 glands from dogs with prostatic hyperplasia. High grade PIN was found in 7 of 20 prostates with carcinoma. Matsuzaki et al (2010) claims to have 5 cases of PIN and examined them by immunohistochemistry. They believe these to be low grade PIN, thus drawing a parallel with the human disease. This study is therefore contradictory to the widely held view of the lack of low grade PIN in dogs. The foci in their study had a higher expression of nuclear p63 and a higher proliferation index (PCNA) than normals. These cells had 'heterogenous' staining with androgen receptor. They surmised that basal cells play a role in the development of canine PIN.

Some prostatic carcinomas have cytogenetic abnormalities and of particular interest is one with a similar abnormality to a human prostatic carcinoma. The carcinoma studies had trisomy of chromosome 13, which is similar to chromosome 8 of humans and which also has cytogenetic anomalies in some human prostatic carcinomas (Winkler et al 2006). This is a recent field of investigaton with the first report being by Winkler et al (2005).

Palmieri (2015) found that carcinomas in the prostate acquire expression of angiogenic factors such as PECAM-1, VEGF and FGF-2.



Akter SH, Lean FZ, Lu J, Grieco V, Palmieri C. Different Growth Patterns of Canine Prostatic Carcinoma Suggests Different Models of Tumor-Initiating Cells. Vet Pathol. 2015 52(6):1027-1033.

Bell RW, Klausner JS, Hayden DW, Feeney DA, Johnston SD (1991) Clinical and pathologic features of prostatic adenocarcinoma in sexually intact and castrated dogs: 31 cases (1970-1987). J Amer Vet Med Asoc 199: 1623-

Cornell KK, Bostwick DG, Cooley DM, Hall G, Harvey HJ, Hendrick MJ, Pauli BU, Render JA, Stoica G, Sweet DC, Waters DJ. (2000) Clinical and pathologic aspects of spontaneous canine prostatic carcinoma: a retrospective analysis of 76 cases. The Prostate 45: 173-183.

Durham SK, Dietze AE (1986). Prostatic adenocarcinoma with and without metastasis to bones in dogs. J Amer Vet Med Assoc 188: 1432-1436.

Gallardo F, Mogas T, Baró T, Rabanal R, Morote J, Abal M, Reventós J, Lloreta J. (2007) Expression of Androgen, Oestrogen a and ß, and Progesterone Receptors in the Canine Prostate: Differences between Normal, Inflamed, Hyperplastic and Neoplastic Glands J Comp Path 136: 1-8

Grieco V, Patton V, Romussi S, Finazzi M. (2003) Cytokeratin and vimentin expression in normal and neoplastic canine prostate. J Comp Path 129: 78-84.

Grieco V, Riccardi E, Rondena M, Romussi S, Stefanello D, Finazzi M. (2006) The distribution of oestrogen receptors in normal, hyperplastic and neoplastic canine prostate, as demonstrated immunohistochemically. J Comp Pathol. 135(1):11-16.

Guerin VJ, Visser 't Hooft KW, L'Eplattenier HF, Petite AF (2012) Transitional cell carcinoma involving the ductus deferens in a dog. J Amer Vet Med Assoc 2012, 240: 446-449

Lai C-L, van den Ham R, van Leenders G, van der Lugt J, and Teske E. (2008) Comparative characterization of the canine normal prostate in intact and castrated animals.The Prostate 2008; 68: 498-507

Lai C-L, van den Ham R, van Leenders G, van der Lugt J, Moll JA, and Teske E. (2008) Histopathological and immunohistochemical characterisation of canine prostate cancer.The Prostate 2008; 68: 477-488

Lai C-L, van den Ham R, Mol J, Teske E (2009) Immunostaining of the androgen receptor and sequence analysis of its DNA-binding domain in canine prostate cancer. The Vet J 181: 256-260

Leav I, Ling GV. (1968) Adenocarcinoma of the canine prostate. Cancer 22: 1329-1345.

LeRoy BE, Nadella MVP, Toribio RE, Leav I, Rosol TJ. (2004) Canine prostate carcinomas express markers of urothelial and prostatic differentiation. Vet Pathol 41: 131-140.

LeRoy BE, Painter A, Sheppard H. Popiolek L, Samuel-Foo M, Andacht TM. (2007) Protein expression profiling of normal and neoplastic canine prostate and bladder tissue. Vet Comp Oncology 5 (2) 119-130.

Madewell BR, Gandour-Edwards R, DeVere White RW. (2004) Canine prostatic intraepithelial neoplasia: is the comparative model relevant? The Prostate m58: 314-317.

McEntee M, Isaacs W, Smith C. (1987) Adenocarcinoma of the canine prostate: immunohistochemical examination for secretory antigens. The Prostate 11: 163-170.

Matsuzaki P, Cogliati B, Sanches DS, Chaible LM, Kimura KC, Silva TC, Real-Lima MA, Hernandez-Blazquez FJ, Laufer-Amorim R, Dagli MLZ (2010) Immunohistochemical Characterization of Canine Prostatic Intraepithelial Neoplasia. J Comp Path 142: 84-88

O'Shea JD (1963) Studies on the canine prostate gland. II Prostatic neoplasms. J Comp Path 73: 244-252

Palmieri C, Lean FZ, Akter SH, Romussi S, Grieco V. A retrospective analysis of 111 canine prostatic samples: histopathological findings and classification. Res Vet Sci. 2014; 97: 568-573.

Palmieri C, Riccardi E. (2013) Immunohistochemical Expression of HOXA-13 in Normal, Hyperplastic and Neoplastic Canine Prostatic Tissue. J Comp Pathol 2013; 149: 417–423

Palmieri C. Immunohistochemical Expression of Angiogenic Factors by Neoplastic Epithelial Cells Is Associated With Canine Prostatic Carcinogenesis. Vet Pathol. 2015; 52: 607-613.

Ravicini S, Baines SJ, Taylor A, Amores-Fuster I, Mason SL, Treggiari E. Outcome and prognostic factors in medically treated canine
prostatic carcinomas: A multi-institutional study. Vet Comp Oncol 2018:

Rodrigues MMP, Rema A, Gärtner F, Soares FA, Rogatto SR, De MourVMBD, Laufer-Amorim R. (2011) Overexpression of Vimentin in Canine Prostatic Carcinoma. J Comp Path 2011 144: 308-311

Taylor PA (1973) Prostatic adenocarcinoma in a adog and a summary of ten cases. Canadian Vet J 14: 162-166.

Teske E, Naan EC, van Dijk EM, Van Garderen E, Schalken JA. (2002) Canine prostate carcinoma: epidemiological evidence of an increased risk in castrated dogs. Mol Cell Endocrinol. 2002 197(1-2):251-255

Waters DJ, Bostwick DG. (1997) Prostatic intraepithelial neoplasia occurs spontaneously in the canine prostate. J Urol 157: 713-716.

Waters DJ, Hayden DW, Bell FW, Klausner JS, Qian J, Bostwick DG. (1997) Prostatic intraepithelial neoplasia in dogs with spontaneouos prostate cancer. (The Prostate 30: 92-97.

Weaver AD (1981) Fifteen cases of prostatic carcinoma in the dog. Vet Rec 109: 71-75.

Winkler S, Murua Escobar H, Eberle N, Reimann-Berg N, Nolte I, Bullerdiek J. (2005) Establishment of a cell line derived from a canine prostate carcinoma with a highly rearranged karyotype. J Hered. 96(7):782-785.

Winkler S, Reimann-Berg N, Escobar HM, Loeschke S, Eberle N, Hoinghaus R, Nolte I, Bullerdiek J. (2006) Polysomy 13 in a canine prostate carcinoma underlining its significance in the development of prostate cancer. Cancer Genet Cytogenet.169(2):154-158

Mesenchymal neoplasia

In a multiinstitutional study of prostatic carcinoma, Cornell et al (2000) examined the records of 228 cases of prostatic neoplasia and reported 3 cases of sarcoma, but there are no other details.

Cornell KK, Bostwick DG, Cooley DM, Hall G, Harvey HJ, Hendrick MJ, Pauli BU, Render JA, Stoica G, Sweet DC, Waters DJ. (2000) Clinical and pathologic aspects of spontaneous canine prostatic carcinoma: a retrospective analysis of 76 cases. The Prostate 45: 173-183.


Hayden et al (1992) reported on a dog with haemangiosarcoma they suggested arose in the prostate and metastasized to multiple organs. There is one case in the Yager-Best Histovet database (YB54561).

Figure : Hemangiosarcoma of prostate.

Hayden DW, Bartges JW, Bell FW, Klausner JS. (1992). Prostatic hemangiosarcoma in a dog: clinical and pathologic findings. J Vet Diagn Invest 4: 2009-211.


Smooth muscle tumor - Leiomyoma - Leiomyosarcoma

Hayden et al (1999) reported a case of leiomyosarcoma in the prostate of a dog.

Bacci et al (2010) reported a case of leiomyosarcoma in the prostate of a dog - it also had pulmonary metastases.

Holdsworth et al (2015) reported on a dog with a leiomyoma of the prostate.

Trovatelli et al (2021) reported on a dog with leiomyosarcoma of the prostate. There were no metastases



Holdsworth A, Bléhaut T, Reeve LDay MJ, Warren-Smith C. An incidental prostatic leiomyoma in a dog. Vet Rec Case Rep 3:e000204 

Bacci B, Vignoli M, Rossi F, Gallorini F, Terragni R, Laddaga EL, and Sarli G. (2010) Primary Prostatic Leiomyosarcoma With Pulmonary Metastases in a Dog. J Am Anim Hosp Assoc 2010;46: 103-106

Hayden DW, Klausner JS, Waters DJ. (1999) Prostatic leiomyosarcoma in a dog. J Vet Diagn Invest. 11(3):283-6.

Trovatelli M, Bassi J, Giudice C, Ferrari R, Longo M, Brizzola S. Prostatic leiomyosarcoma in a dog treated using a multimodal approach. J Vet Intern Med. 2021


One case of osteosarcoma of the prostate is mentioned by in a discussion of cases with obstruction of the urethra by Weisse et al (2006). It had pulmonary metastases.

Weisse C, Berent A, Todd K, Clifford C, Solomon J. (2006) Evaluation of palliative stenting for management of malignant urethral obstructions in dogs. J Amer Vet Med Assoc 229: 226-234.


Mainwaring (1990) reported a case of lymphoma that only was found in the prostate and adrenal. It was considered a primary prostatic lymphoma. There is one case of lymphoma of the prostate in the Yager-Best Histovet database (YB52270).

Mainwaring CJ (1990) Primary lymphoma of the prostate on a dog.J Small Anim Pract 31: 617-619

Prostatic and paraprostatic cysts

There are many cysts that can and do develop within and around the prostate. Those around the prostate are lumped together as paraprostatic cysts. Hoffer et al (1977) classified prostatic cysts into 4 groups, and an additional one is added

Hoffer RE, Dykes NL, Greiner TP (1977) Marsupialization as a treatment for prostatic disease. J Amer Anim Hosp Assoc 13: 98-104.

Bloom F (1954). "Pathology of the Dog and Cat: The genitourinary system, with clinical considerations" Am. Vet. Publ Evanston, Illinois

The grouping here is based on the basic separation of those cysts within the prostate and those outside it..

Multiple cysts in prostatic hyperplasia

During age associated prostatic hyperplasia in intact male dogs there is variable distension of prostatic acini to form cystic structures. Some of these distended lumens are large enough to be classified as cysts, and grossly some are several centimeters in diameter.Black et al (1998) found that of 85 dogs with no indication of prostatic disease, 12 had prostatic cysts that ranged from 1.5 to 2.4 cm diameter. 5 of the 12 had positive cultures for bacteria or mycoplasma. Some of these prostates have a polycystic gross appearance. Histologically these cysts are lined by normal glandular cells. When there is rapid elargement of the cysts, the epithelium may become attenuated.

.Black GM, ling GV, Nyland TG, Baker T (1998) Prevalence of prostatic cysts in adult large breed dogs. J Amer Anim Hosp Assoc 34: 177-180.

Paraprostatic lymphatic cysts

Multiple thin fluid filled cysts are found in old dogs with prostatic hyperplasia. They are lined by flattened endothelial cells.

Bloom F (1954). "Pathology of the Dog and Cat: The genitourinary system, with clinical considerations" Am. Vet. Publ Evanston, Illinois

McEntee K (1990) Reproductive Pathology of Domestic Mammals, Academic Press p338.

Paraprostatic cysts and pseudocysts

The most common 'cyst' biopsied and submitted is the paraprostatic pseudocyst, and these can assume enormous proportions. Some can be up to 30cm in diameter (or larger) and form a space occupying mass in the abdomen. It is not known how or from what they arise. Some have a higher creatinine concentration than serum and thus contain urine. These are known as 'urine cysts' or 'prostatic cavitary lesions containing urine' (Bokemeyer et al 2011). Bokemeyer et al (2011) found that about 18% of prostatic or paraprostatic cysts contained higher creatinine and therefore urine. Communication of the cyst with the duct of the prostate and therefore the urethra would be responsible.

Some cysts, particularly the smaller ones, are lined by epithelium and they may communicate with prostatic cysts and acini. Many prostates have projections of glands from the prostate into and through the capsule - and they are seen to extend between bundles of the discontinuous smooth muscle of the capsule. It is likely that many paraprostatic cysts are an extension of cysts in prostatic hyperplasia.

Other possible origins for paraprostatic cysts are serosal inclusion cyst and hematomas (McEntee 1990).

Those that are in the dorsal midline region of the prostate are assumed to be derived from a cystic uterus masculinus, a remnant of the paramesonephric duct.

The structure of the cysts make determining their origin impossible as the inner lining is seldom lined by epithelium. The term pseudocyst is more precise in this instance. The lining is often either fibrous or granulation tissue with an appearance similar to a 'seroma'. The wall is usually of compressed fibrous tissue and the outer lining is mesothelium (serosa).

It is not unusual for the pseudocysts to have mineralisation of the wall, although the literature is scant on this (Girard and Despots 1995, Head and Francis 2002).

It is possible for prostatic cysts to herneate through the inguinal ring. (Vittitoe et al 2017)

The pseudocysts are readily recognised clinically, but are difficult to manage. Some can become infected and become abscesses. There are 9 paraprostatic cysts diagnosed in the Yager-Best Histovet database - 2 had mineralization/ossification and 1 was abscessed.

Figure : Paraprostatic pseudocyst. Bladder is to the right and prostate is lower left.

Figure : Paraprostatic pseudocyst. The inner lining is granulation tissue with no epithelium.

Figure : Paraprostatic pseudocyst. The inner lining is lower left, the ossified portion is central, the dense fibrous wall and serosa is upper right.

Bokemeyer J, Peppler C, Thiel C, Failing K, Kramer M, Gerwing M. (2011) Prostatic cavitary lesions containing
urine in dogs. J Small Anim Pract 2011 52: 132-138.

Girard C, Despots J (1995). Mineralized paraprostatic cyst in a dog. Canadian vet J 36: 573-574.

Head LL Francis DA (2002). Mineralized paraprostatic cyst as a potential contributing factor in the development of perineal hernias in a dog. J Am Vet Med Assoc 221(4): 533-535.

McEntee K (1990) Reproductive Pathology of Domestic Mammals, Academic Press p338

Vititoe KP, Grosso FV, Thomovsky S, Lim CK, Heng HG. Inguinal herniation of a mineralized paraprostatic cyst in a dog. Can Vet J. Can Vet J. 2017; 58: 1309-1312.

Weaver AD (1978). Discrete prostatic (paraprostatic) cysts in the dog.


Prostatitis and prostatic abscess

Inflammation of the prostate is called prostatitis. Sequential studies of prostatitis are lacking, so much is assumed from studies in other animals. Prostatitis is a common finding, even in asymptomatic dogs (Diniz et al 2005). It is reported to occur in canine brucellosis (Brennan et al 2008).

Lea et al (2022) collected 82 clinical cases. Micturition disorders were identified in 52 of 82 cases and those with acute prostatitis had pyrexia. They separated the dogs into those with clinical systemic signs (acute) and without systemic signs (chronic). It was an incidental finding in 7 of 30 considered chronic prostatitis.

Prostatitis should not occur in dogs neutered in puppyhood. It is reported in a neutered 10 yrs old dog that was castrated at 5 yrs (Duque et al 2010). This dog had prostatic cysts too, so it is likely that preexistent disease became clinical later in life. Lea et al (2022) in their clinical study, found prostatitis in 65 intact dogs of 82 cases submitted to a referral practice. That left 17 neutered dogs with prostatitis. The age of neuter was not provided. Of the many cases I have seen, only 1 was in a dog neutered in puppyhood - the rest were in dogs neutered as adults.

Many dogs have foci of inflammatory cells in the interstitial tissues (James and Heywood 1979), suggesting that subclinical infection may be common. 10% of dogs had these at 6 months but 45% had them at 7 years.

Duque J, Macías-García B, Ruíz Tapia P, Ortega Ferrusola C, Zaragoza C, Barrera R, Peña FJ. (2010) Two Unusual Cases of Canine Prostatitis: Prostatitis in a Castrated Dog and Preputial Oedema in an Intact Male Reprod Dom Anim 2010 45: e199-e200

Lea C, Walker D, Blazquez CA, Zaghloul O, Tappin S, Kelly D. Prostatitis and prostatic abscessation in dogs: retrospective study of 82 cases. Aust Vet J. 2022; 100: 223-229.


It is assumed that prostatis occurs mostly by ascending infection - organisms travel from the penis and prepuce via the urethra to the prostate. Hematogenous spread and localisation in the prostate is probably the way that infection with Brucella reaches the prostate, but infection from epididymitis is also possible. There is also the theoretical possibility of infection of the prostate from the bladder and urine.

Once bacteria infect the prostate, it is likely they grow within the lumen of the glands, and from there either elicit an inflammatory response or invade. It is therefore likely that ascending infection will have an acute intraacinar or glandular phase and later an interstitial phase. Bacteria within the lumen of the glands will likely not be recognised by the body, at least not initially. Neutrophils and the contents of their granules will contribute to the chemotactic factors of the bacteria to encite an inflammatory response. Bacteria would likely be Gram negative and therefore release endotoxin. With time, the interstitial response will become more obvious, with lymphocytes and plasma cells predominating. This interstitial phase will also be accompanied with fibrosis.

Abscessation of the prostate is one outcome of prostatitis. Prostatic abscesses will be discussed separately.

Macroscopic findings

Acute severe prostatitis is a painfull condition that is usually accompanied by systemic illness. Such cases will have edema and hemorrhage of the prostatic and periprostatic tissues. It is difficult to determine the outline of the prostate because of this acute inflammatory response.

Figure : Severe acute prostatitis. There is marked periprostatic edema and haemorrhage.

When the inflammatory response is suppurative, the prostate will be uniformly enlarged and pus will exude from the cut surface, especially when there is pressure applied to the prostate.

Chronic prostatitis will have a firm white appearance, or have no macroscopic changes visible.

On rare occasions, prostatis can be emphysematous (Rohleder and Jones 2002)

Microscopic findings.

In the most severe forms of prostatitis, there is extensive edema and hemorrhage that separate the interstitial tissues and widely separate acini from each other. Necrosis of portions of the prostate can be expected. Neutrophils will be the predominant inflammatory cell - both in the intersitium and within the acini. In the less severe examples, neutrophils, macrophages and necrotic debris will be in the lumens, and cause them to be distended. The interstitium, initially will contain neutrophils, but with time, lymphocytes and plasma cells will appear around the acini and around vessels. Fibrosis will develop as well. Atrophy of glands in the areas near inflammation may occur. Some believe this atrophy is prostatic proliferative inflammatory atrophy. The evidence of proliferation and the suggestion of this being a preneoplastic lesion in dogs is in its infancy and not supported by current research.

Figure : Chronic interstitial prostatis.

Figure : Chronic interstitial prostatitis

Figure : Chronic intestitial prostatitis


Palmieri C, Story MLean FZX, Akter SH, Grieco V. De Marzo AM. Diagnostic Utility of Cytokeratin-5 for the Identification of Proliferative Inflammatory Atrophy in the Canine Prostate J Comp Pathol 2018; 158: 1-5

Bacterial prostatitis

There is surprisingly little infomation about the kinds of bacteria involved in prostatis in dogs. Brucella sp infection of the prostate is a well recognized entity and will be discussed below.

The bacteria isolated from cases of prostatitis include Escherichia coli, Proteus, Klebsiella, Staphylococcus, Streptococcus sp, but there is little information on prevalence.

There is one case report of emphysematous prostatitis from which Escherichia coli was cultured. (Rohleder and Jones 2002).

Brucella prostatitis

Prostatitis is part of canine brucellosis, although it may not be clinically evident. The prostatitis tends to be of the chronic interstitial type, although this probably reflects the fact that the lesions take a long time to develop and the acute phase is over. Brucells canis, Brucella suis and Brucella abortus are all capable of causing prostatitis in dogs (Barr et al 1986)

Brennan et al (2008) wrote about brucellosis in a kennel in Saskatchewan. The lesions they found in 5 male dogs with titres to Brucella sp (presumabley B canis) were epididymitis and prostatitis in one dog, prostatitis and in 4 of the 5. dogs. The lesions were of the interstitial type.

Olsen and Palmer (2015) provides a detailed review of the pathogenesis and pathology of brucellosis in all species.

Barr SC, Eitis BE, Roy AF, Miller R. (1986). Brucella suis biotype 1 infection in a dog. J Amer Vet Med Assoc 189: 686-687.

Brennan SJ, Ngeleka M, Philibert HM, Forbes LB, Allen AL (2008) Canine brucellosis in a saskatchewan kennel. Canadian Vet J 49: 703-708

Mycotic prostatitis

Granulomatous prostatitis occurs in dogs with infection with Blastomyces dermatiditis, Cryptococcus neoformans and Coccidiodes immitis (Johnston et al 2000).

Reed et al (2010) describe a case of granulomatous prostatitis due to Blastomyces dermatitidis.

Totten et al (2011) reported on 4 clinical cases of blastomycosis where the prostate was involved. They examined 155 dogs with blastomycosis of which 86 were male and 37 were intact. 4 had their testes examined and all blastomycosis. 4 of the dogs had prostatic involvement and diagnosis was on fine needle aspirant cytology. None of the dogs with testicular involvement had evaluation of their prostate.


Tiffany Reed, Kelley A. Balog, Katie M. Boes, Joanne B. Messick, and Margaret A. Miller (2010) Pathology in Practice: J Amer Vet Med Assoc 2010, 236: 411-413.

Totten AK, Ridgway MD, Debra S. Sauberli DS. (2011) Blastomyces dermatitidis Prostatic and Testicular Infection in Eight Dogs (1992–2005). J Am Anim Hosp Assoc 2011, 47: 413-418


L'Abee-Lund et al (2003) report the recovery by culture of Mycoplasma canis from a dog with prostatitis.

L'Abee-Lund TM, Heiene R, Friis NF, Ahrens P, Sorum H (2003) Mycoplasma canis and urogenital disease in dogs in Norway. Vet Rec. 2003 153(8):231-235.


James RW, Heywood R. (1979) Age-related variations in the testes and prostate of beagle dogs. Toxicology. 12(3):273-279.

Johnston SD, Kamolpatana K, Root-Kustritz MV, Johnston GR (2000) Prostatic disorders in the dog. Anim Reprod Sci. 60-61:405-415

Protozoal prostatitis

It is known that dogs with Leishmanosis can shed organisms in their semen, and that inflammation of the genital organs occurs when dogs have visceral involvement (Diniz et al 2005). Mir et al (2012) reports on a stud dog with prostatits and infertility related to infection with a Leishmania.

Diniz SA, Melo MS, Borges AM, Bueno R, Reis BP, Tafuri WL, Nascimento EF, Santos RL. (2005) Genital Lesions Associated with Visceral Leishmaniasis and Shedding of Leishmania sp. in the Semen of Naturally Infected Dogs Vet Pathol 42: 650-658.

Mir F, Fontaine E, Reyes-Gomez E, Carlus M, Fontbonne A. (2012) Subclinical leishmaniasis associated with infertility and chronic prostatitis in a dog. J Small Anim Pract 2012, 53: 419-422

Prostatic abscess

Prostatic abscesses are inflammatory lesions where there is the formation of a cavity filled with pus. The size of the 'normal' prostate is sufficiently small that infection and necrosis with the formation of an abscess is unlikely. It is much easier to imagine an abscess developing in a prostatic cyst, and there is often a background of prostatic hyperplasia to acheive this. Paraprostatic pseudocysts are sites for the development of 'prostatic abscesses' although these should be called paraprostatic abscesses.

Figure : Prostatic abscess. The abscess is opened (upper) and the cut surface of the hyperplastic prostate is visible. Bladder is center right.

Rohleder JJ, Jones JC (2002) Emphysematous prostatitis and carcinoma in a dog J Am Anim Hosp Assoc. 38(5): 478-481

Miscellaneous conditions of the prostate

Prostatic corpora amylacea

Corpora amylacea are usually incidental histologically apparent concretions in the acini of glands. They are composed of concentrically arranged lines and they stain with PAS. They are seen periodically in older dogs (McEntee 1990).

McEntee K (1990) Reproductive Pathology of Domestic Mammals, Academic Press p339.

Prostatic calculi

Calculi of the prostate are mineralized concretions that may be found in the prostate. They may be macroscopically visible, but some are microscopic. Lumb (1952) reports one case and McEntee (1990) has seen them in 3 dogs.

Lumb WV. (1952) Prostatic calculi in a dog. J Am Vet Med Assoc. 121:14-16.

McEntee K (1990) Reproductive Pathology of Domestic Mammals, Academic Press p339.

Osseous metaplasia of prostate

One case of mineralisation and osseous metaplasia of the prostate is reported (Aughey and Weaver 1977)

Aughey E, Weaver AD. (1977) Calcification of the prostate gland of the dog. Zentralbl Veterinarmed A. 24(9):772-778.

Inadvertent prostatectomy

There are multiple individual case reports about veterinarians who, when attempting to remove a cryptorchid testis, trace the deferent duct to a nodule that they subsequently remove. The nodule is the prostate! Obstruction of the urethra and uroabdomen often follow!!!

Puttick JL, Sereda CW. (2012) Suture related urolithiasis following repair of inadvertent prostatectomy in a dog. Can Vet J 2012, 53: 787-790